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References to Pulmonary Barotrauma
J Emerg Med 1998 May-Jun;16(3):413-7
Fatal pulmonary barotrauma due to obstruction of the central circulation with air.
Neuman TS, Jacoby I, Bove AA
Hyperbaric Medicine Center and Department of Emergency Medicine,
of California Medical Center, San Diego, USA.
Cardiac arrest in cases of barotraumatic arterial gas embolism (AGE)
ascribed to reflex dysrhythmias secondary to brainstem embolization or secondary
to coronary artery embolization. Several case reports suggest that obstruction of
the central circulation (i.e., the heart, pulmonary arteries, aorta, and arteries to the
head and neck) may play a role in the pathogenesis of sudden death in victims of
pulmonary barotrauma. We report three consecutive cases of fatal AGE in patients
in whom chest roentgenograms demonstrated confluent air lucencies filling the
central vascular bed, the heart, and great vessels. In none of the victims was there
evidence by history or at autopsy that the intravascular gas was iatrogenically
introduced. Total occlusion of the central vascular bed with air is a mechanism of
death in some victims of AGE, and resuscitation efforts for such patients should take this possibility into consideration.
Undersea Hyperb Med 1997 Winter;24(4):301-8
Recompression treatments during the recovery of TWA Flight 800.
Leffler CT, White JC
Medical Department, Naval Amphibious Base Little Creek, Virginia, USA.
After the crash of TWA flight 800, U.S. Navy (USN) and civilian
the aircraft and the victims' remains from 117 feet of sea water (fsw). Safety
information was gathered from observations, interviews, and medical and diving
records. Of 752 dives employing surface decompression using oxygen (SDO2), 10
divers required recompression treatments, mainly for type 2 decompression
sickness (DCS). When using hot water heating, the DCS risk was high until the
dive profiles were modified. Divers made nearly 4,000 no-decompression scuba
dives. In eight scuba divers and one tender treated with recompression, the
diagnoses included DCS (3), arterial gas embolism (AGE) (1), and vascular
headache (2). All USN divers recovered fully. The experience is consistent with
previous work suggesting an increase in DCS risk in warmer SDO2 divers. The
USN SDO2 tables can be made safer by limiting bottom time and extending
decompression. Even under stressful conditions, rapid ascents resulting in AGE are
uncommon. Vascular headaches can mimic DCS by responding to oxygen.
Aviat Space Environ Med 1997 Nov;68(11):1025-8
Neurological manifestation of arterial gas embolism following standard altitude chamber
flight: a case report.
Rios-Tejada F, Azofra-Garcia J, Valle-Garrido J, Pujante Escudero A
Centro de Instruccion de Medicina Aeroespacial (C.I.M.A.), Madrid, Spain.
In the course of a decompression at flight level 280 (28,000 ft) in
chamber flight, a 45-yr-old cabin air traffic controller developed sudden numbness
in his left upper and lower extremities and, soon after, complete paralysis in the
left side, dysarthria and left facial palsy. A presumptive diagnosis of arterial gas
embolism (AGE) was made and hyperbaric oxygen therapy (HBO) was given after
airevac of the patient to the closest compression facility. Complete resolution of
the symptoms was obtained after treatment Table VI-A (extended), plus 3
consecutive HBO treatments (90 min of Oxygen at 2.0 ATA). AGE is a rare event
in the course of regular altitude chamber flight and diagnosis should be done in the
context of the barometric pressure changes and an acute cerebral vascular injury.
Risk factors and follow-up diagnostic procedures are discussed.
Chest 1997 Sep;112(3):654-9
Risk factors for pulmonary barotrauma in divers.
Tetzlaff K, Reuter M, Leplow B, Heller M, Bettinghausen E
Department of Diving and Hyperbaric Medicine, Naval Medical Institute, Kiel,
STUDY OBJECTIVES: Pulmonary barotrauma (PBT) of ascent is a feared
complication in compressed air diving. Although certain respiratory conditions are
thought to increase the risk of suffering PBT and thus should preclude diving, in
most cases of PBT, risk factors are described as not being present. The purpose of
our study was to evaluate factors that possibly cause PBT. DESIGN: We analyzed
15 consecutive cases of PBT with respect to dive factors, clinical and radiologic
features, and lung function. They were compared with 15 cases of decompression
sickness without PBT, which appeared in the same period. RESULTS: Clinical
features of PBT were arterial gas embolism (n=13), mediastinal emphysema
(n=1), and pneumothorax (n=1). CT of the chest (performed in 12 cases) revealed
subpleural emphysematous blebs in 5 cases that were not detected in preinjury and
postinjury chest radiographs. A comparison of predive lung function between
groups showed significantly lower midexpiratory flow rates at 50% and 25% of
vital capacity in PBT patients (p<0.05 and p<0.02, respectively).
CONCLUSIONS: These results indicate that divers with preexisting small lung
cysts and/or end-expiratory flow limitation may be at risk of PBT.
Ernest Campbell, MD, FACS All Rights Reserved.